Typically, most athletic endeavors involve elements of all three. The learning aspect of training involves motivational factors, as well as neuromuscular coordination. This aspect of training does not involve adaptive changes in the muscle fibers per se. However, motor skills can persist for years without regular training, unlike the responses of muscle cells to exercise.
All healthy persons can maintain some level of continuous muscular activity that is supported by oxidative metabolism. This level can be greatly increased by a regular exercise regimen that is sufficient to induce adaptive responses. The adaptive response of skeletal muscle fibers to endurance exercise is mainly the result of an increase in the oxidative metabolic capacity of the motor units involved. This demand places an increased load on the cardiovascular and respiratory systems and increases the capacity of the heart and respiratory muscles. The latter effects are responsible for the principal health benefits associated with endurance exercise.
Muscle strength can be increased by regular massive efforts that involve most motor units. Such efforts recruit fast glycolytic motor units, as well as slow oxidative motor units. During these efforts, blood supply to the working muscles may be interrupted as tissue pressures rise above intravascular pressure. The reduced blood flow limits the duration of the contraction. Regular maximal-strength exercise, such as weightlifting, induces the synthesis of more myofibrils and hence hypertrophy of the active muscle cells. The increased stress also induces the growth of tendons and bones.
Endurance exercise does not cause fast motor units to become slow, nor does maximal muscular effort produce a shift from slow to fast motor units. Thus any practical exercise regimen, when superimposed on normal daily activities, probably does not alter muscle fiber phenotype.
Activities such as hiking or, in particular, downhill running, in which contracting muscles are stretched and lengthened too vigorously, are followed by more pain and stiffness than after comparable exercise that does not involve vigorous muscle stretching and lengthening (e.g., cycling). The resultant dull, aching pain develops slowly and reaches its peak within 24 to 48 hours. The pain is associated with reduced range of motion, stiffness, and weakness of the affected muscles. The prime factors that cause the pain are swelling and inflammation from injury to muscle cells, most commonly near the myotendinous junction. Type II motor units are affected more than type I motor units because the maximal force is highest in large cells, in which the loads imposed are approximately 60% greater than the maximal force that the cells can develop. Recovery is slow and depends on regeneration of the injured sarcomeres.
Biophysical Properties of Skeletal Muscle
The molecular mechanisms of muscle contraction described earlier underlie and are responsible for the biophysical properties of muscle. Historically, these biophysical properties were well described before elucidation of the molecular mechanisms of contraction. They remain important ways of describing muscle function.
When muscles contract, they generate force (often measured as tension or stress) and decrease in length. In examination of the biophysical properties of muscle, one of these parameters is usually held constant, and the other is measured after an experimental maneuver. Accordingly, an isometric contraction is one in which muscle length is held constant, and the force generated during the contraction is then measured. An isotonic contraction is one in which the force (or tone) is held constant, and the change in length of the muscle is then measured.
When a muscle at rest is stretched, it resists stretch by a force that increases slowly at first and then more rapidly as the extent of stretch increases (